Central respiratory adaptation is the mechanism by which the central nervous system maintains physiologically appropriate blood pH and gas levels via changes in breathing. The central chemoreception is poorly understood. Here we investigated the role of task2 potassium channels for the control of respiration. Task2 expression in the central nervous system is unique and strictly restricted to few brainstem nuclei, particularly to the retrotrapezoid/parafacial region. We observed that mice invalidated for the task2 K⁺channel gene had lost the long-term hypoxia-induced respiratory decrease while the acute carotid body-mediated increase was maintained. The response to changes in CO₂ was modified in knockout mice. In the isolated brainstem-spinal cord preparation, the anoxia-induced respiratory depression was absent in task2-/- mice demonstrating the central origin of this phenotype. These data identify task2 channels as an important determinant of central chemoreception and demonstrate that this phenomenon is due to the activity of a very small number of neurons located in the ventral medullary surface.